(1) MAIDS is a lymphoproliferative, immunosuppressive disease of C57BL/6 mice caused by a replication-defective c-type retrovirus (LP-BM5). Adherent cells isolated from the peritoneal cavity and seminal fluid of infected mice were examined by electron microscopy and FACS. Greater than 90% of adherent cells were of macrophage morphology and phenotype. They were found to be expressing virus as early as 1 week after virus inoculation with the number of infected cells rising as disease progressed. As few as 10^5 adherent cells from infected mice were capable of inducing disease in 100% of naive mice when injected I.P. These studies show that cells of the macrophage/monocyte lineage are an important reservoir for LP-BM5 and may be involved in the sexual transmission of MAIDS. (2) U937 cells were exposed to either standard Sendai virus stock (St) or to one containing St and defective interfering particles (StDi). Electron microscopic analysis showed that infection with St leads to the abundant synthesis of nucleocapsid material in the cytoplasm of most cells. Production of extracellular, formed viral particles, however, is small. Despite the substantial burden of viral products, cells appear relatively healthy and the eventual death of heavily infected cells occurs by necrosis. In contrast, infection with StDi results in very little nucleocapsid synthesis in most cells. Nonetheless these cultures exhibit a conspicuous early CPE consisting of the widespread disintegration of many cells by the mechanism of apoptosis (programmed cell death). Apoptosis differs fundamentally from necrosis as a mechanism of cell death. DI particles have not, until now, been shown to be capable of triggering this mechanism. (3) In cooperation with the Division of Transfusion Science, liver biopsies of experimentally infected chimps are prepared for EM and examined for evidence of infection by hepatitis C virus.